Reply to Schoppman et al.

• Endoscopic RFA
• Barrett esophagus, cardiorespiratory illness and metabolic syndrome
• References

We were delighted to read the interesting letter from Professor Schoppman and colleagues. They raise two issues: pre-emptive endoscopic radiofrequency ablation (RFA) to prevent development of esophageal adenocarcinoma (EAC); and the link between Barrett’s esophagus, cardiorespiratory illness, and metabolic syndrome.

In our cohort [1], 24 % died during follow-up, and of those 16 % died from EAC, compared with 34 % from cardiovascular causes. Overall mortality was higher than expected but only due to EAC.

Endoscopic RFA

RFA is effective in removing the Barrett’s epithelium and may reduce the risk of progression to EAC. However for those with no dysplasia the benefit is unclear; hence the position of the American Gastroenterology Association is not to intervene in this group [2] and many countries have not licenced RFA for use in nondysplastic Barrett’s esophagus. Balancing the hazards of the procedure against its benefits prompts the question: who is at risk of developing EAC? Risk stratification within patients with Barrett’s esophagus remains an attractive prospect, allowing resources to be concentrated on those patients most at risk.

Sikkema et al. in 2011 have used low grade dysplasia (LGD) as a pivotal point for risk stratification [3]. However, their diagnostic criteria were rigid, involving confirmation by a national expert pathologist. In routine clinical practice, the degree of intraobserver variation in LGD diagnosis is well recognized. We certainly need ways of reliably identifying those at risk who will benefit most from endoscopic intervention, which in the years ahead will become progressively more effective, safe, and available. For example, identifying those with the risk factor of blood group O rhesus D negative is a simple step [4]. Of course, the ultimate in risk stratification is the identification of reliable molecular markers and we are working with colleagues at Harvard to this end.

Barrett esophagus, cardiorespiratory illness and metabolic syndrome

Higher body mass index (BMI) is associated both with reflux and cardiovascular disease; indeed we have ourselves wondered whether an underlying “metabolic syndrome”/insulin resistance is the common link. The “link” with chronic respiratory disease is more difficult. We are increasingly aware of the “extraesophageal reflux” [5] that some with chronic respiratory disease also have, but we cannot separate this from the respiratory legacy in the area of Rotherham from its coal mining and steel industry history. Regrettably therefore, our data do not allow us to explore further Professor Schoppman’s interesting suggestion.

The absence of an increase in the rate of deaths from cardiovascular disease within this cohort does not support specific interventions for cardiovascular risk.

Competing interests: None.

• References

• 1 Caygill CPJ, Royston C, Charlett A et al. Mortality in Barrett’s esophagus: three decades of experience at a single center. Endoscopy 2012; 44: 892-898
  Thieme ConnectPubMedSearch in Google Scholar
• 2 Spechler SJ. Barrett’s esophagus without dysplasia: wait or ablate?. Dig Dis Sci 2011; 56: 1926-1928
  CrossrefPubMedSearch in Google Scholar
• 3 Sikkema M, Looman CWN, Steyerberg EW et al. Predictors for neoplastic progression in patients with Barrett’s esophagus: a prospective cohort study. Am J Gastroenterol 2011; 106: 1231-1238
  CrossrefPubMedSearch in Google Scholar
• 4 Caygill CPJ, Royston C, Charlett A et al. Barrett’s, blood groups and progression to oesophageal cancer: is nitric oxide the link?. Eur J Gastroenterol Hepatol 2011; 23: 801-806
  CrossrefPubMedSearch in Google Scholar
• 5 Bardhan KD, Strugala V, Dettmar PW. Reflux revisited: advancing the role of pepsin. Int J Otolaryngol 2012; 646901 Epub 2011 Nov 10
  PubMedSearch in Google Scholar

Corresponding author

• References

• 1 Caygill CPJ, Royston C, Charlett A et al. Mortality in Barrett’s esophagus: three decades of experience at a single center. Endoscopy 2012; 44: 892-898
  Thieme ConnectPubMedSearch in Google Scholar
• 2 Spechler SJ. Barrett’s esophagus without dysplasia: wait or ablate?. Dig Dis Sci 2011; 56: 1926-1928
  CrossrefPubMedSearch in Google Scholar
• 3 Sikkema M, Looman CWN, Steyerberg EW et al. Predictors for neoplastic progression in patients with Barrett’s esophagus: a prospective cohort study. Am J Gastroenterol 2011; 106: 1231-1238
  CrossrefPubMedSearch in Google Scholar
• 4 Caygill CPJ, Royston C, Charlett A et al. Barrett’s, blood groups and progression to oesophageal cancer: is nitric oxide the link?. Eur J Gastroenterol Hepatol 2011; 23: 801-806
  CrossrefPubMedSearch in Google Scholar
• 5 Bardhan KD, Strugala V, Dettmar PW. Reflux revisited: advancing the role of pepsin. Int J Otolaryngol 2012; 646901 Epub 2011 Nov 10
  PubMedSearch in Google Scholar